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TGF-beta contributes to the shift toward Th2-type responses through direct and IL-10-mediated pathways in tumor-bearing mice.

H Maeda and A Shiraishi
J Immunol January 1, 1996, 156 (1) 73-78;
H Maeda
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A Shiraishi
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Abstract

In previous reports, we showed that tumor-derived TGF-beta induced overproduction of IL-10, and these suppressive cytokines caused macrophage suppression in EL4-bearing mice. Proliferation of T cells from EL-4, but not IL-2, whereas T cells from normal mice were responsive to IL-2. A balance between Th1- and Th2-type cytokine production in EL4-T in response to anti-CD3 Ab or phorbor myristate acetate plus A23187 shifted toward the Th2 dominant pattern. The prevention of TGF-beta and IL-10 activates in vivo by administration of anti-IL-10 Ab (anti-IL-10) or anti TGF-beta Ab (anti-TGF-beta) resulted in the reduction in EL4-T of both IL-4 dependent proliferation and Th2-dominant cytokine production induced by anti-CD-3 stimulation. In addition, the anti-TGF-beta treatment resulted in complete restoration in EL4-T of suppressed IL-2 responsiveness, IL-2R expression, and Th1-type cytokine production, whereas the anti-IL-10 treatment produced partial recovery. These results lead us to conclude that TGF-beta drives the shift in the Th1/Th2 balance toward Th2 via IL-10-mediated development of the Th2 responses and via inhibition of the Th1-type responses directly in EL4-bearing mice.

  • Copyright © 1996 by American Association of Immunologists

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The Journal of Immunology
Vol. 156, Issue 1
1 Jan 1996
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TGF-beta contributes to the shift toward Th2-type responses through direct and IL-10-mediated pathways in tumor-bearing mice.
H Maeda, A Shiraishi
The Journal of Immunology January 1, 1996, 156 (1) 73-78;

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TGF-beta contributes to the shift toward Th2-type responses through direct and IL-10-mediated pathways in tumor-bearing mice.
H Maeda, A Shiraishi
The Journal of Immunology January 1, 1996, 156 (1) 73-78;
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Print ISSN 0022-1767        Online ISSN 1550-6606